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ABSITE 2019-RM > Chapter 23: Parathyroid > Flashcards

Chapter 23: Parathyroid Flashcards

1
Q

Where are the superior parathyroids found?

A

Lateral to the recurrent laryngeal nerves (RLNs), posterior surface of superior portion of gland, above inferior thyroid artery

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2
Q

Superior parathyroids develop from what

A

4th pharyngeal pouch; associated with thyroid complex

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3
Q

Inferior parathyroids develop from what

A

3rd pharyngeal pouch; associated with thymus

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4
Q

Where are the inferior parathyroids found?

A
  • Medial to RLNs, more anterior, below inferior thyroid artery
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5
Q

Parathyroids: which ones are more likely to have a variable location and more likely to be ectopic?

A

Inferior parathyroids

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6
Q

Where are the inferior parathyroids occasionally found?

A

In the tail of the thymus (most common ectopic site) and can migrate to the anterior mediastinum

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7
Q

Ectopic sites of inferior parathyroids

A

Tail of thymus, anterior mediastinum, intra-thyroid, near tracheoesophageal groove

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8
Q

% population that have all parathyroid glands

A

90%

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9
Q

Artery: blood supply to both superior and inferior parathyroid glands

A

Inferior thyroid artery

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10
Q

Increases serum calcium

A

PTH

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11
Q

Four physiologic effects of PTH

A
  • Increases kidney Ca reabsorption in the DCT, decreases kidney PO4 absorption
  • Increased osteoclasts in bone to release Ca (and PO4-)
  • Increased VitD production in kidney (increased 1-OH hydroxylation) -> increased Ca-binding protein in intestine -> increased intestinal Ca absorption
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12
Q

Increases intestinal Ca and PO4 absorption by increasing calcium-binding protein

A

Vitamin D

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13
Q
  • Decreases serum Ca
  • Decreases Ca resorption (osteoclast inhibition)
  • increases urinary Ca and PO4 excretion
A

Calcitonin

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14
Q

Normal Ca level

A

8.5 - 10.5 (ionized 4.4 - 5.5)

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15
Q

Normal PTH level

A

5 - 40 pg/mL

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16
Q

Normal PO4 level

A

2.5 - 5.0

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17
Q

Normal Cl- level

A

98 - 107

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18
Q

Most common cause of hypoparathyroidism

A

Previous thyroid surgery

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19
Q
  • Women, older age

- Due to autonomously high PTH

A

Primary hyperparathyroidism

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20
Q

Dx: primary hyperparathyroidism

A

Increased Ca, decreased PO4-, Cl- to PO4- ratio > 33; increased renal cAMP; HCO3- secreted in urine

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21
Q

ABG in primary hyperparathyroidism

A

Hyperchloremic metabolic acidosis

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22
Q

Bone lesions from Ca resorption; characteristic of hyperparathyroidism

A

Osteitis fibrosa cystica (brown tumors)

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23
Q

Symptoms of primary hyperparathyroidism

A

Most patients have no symptoms -> increased calcium found on routine lab work for some other problem or on checkup

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24
Q

Muscle weakness, myalgia, nephrolithiasis, pancreatitis, PUD, depression, bone pain, pathologic fractures, mental status changes, constipation, anorexia

A

Primary hyperparathyroidism

- HTN can result from renal impairment

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25
Q

Diagnostic workup for primary hyperparathyroidism

A
  • H&P. Elevated Ca thru 2-3 detrminations.
  • CXR: look for bony mets, sarcoid, pulmonary tumors
  • Excretory urogram: nephrolithiasis, renal tumors
  • Serum protein electrophoresis to r/o multiple myeloma
  • 24-hr urinary ca determination
  • r/o MEN
  • Check PTH level
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26
Q

Indications for surgery: primary hyperparathyroidism

A
  • Symptomatic disease

- Asymptomatic disease with Ca > 13, decreased Cr clearance, kidney stones, substantially decreased bone mass

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27
Q

Primary hyperparathyroidism: % pts with single adenoma

A

80% of patients

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28
Q

Primary hyperparathyroidism: % pts with multiple adenomas

A

Occur in 4% of patients

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29
Q

Primary hyperparathyroidism: % patients with diffuse hyperplasia

A

Occurs in 15% of patients with MEN 1 or 2a have 4-gland hyperplasia

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30
Q

Hyperparathyroidism: very rare, can get high Ca levels

A

Parathyroid adenocarcinoma

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31
Q

Treatment: parathyroid adenoma

A

Resection; inspect other glands to rule out hyperplasia or multiple adenomas

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32
Q

Treatment: parathyroid hyperplasia

A
  • Do not biopsy all glands -> risks hemorrhage and hypoparathyroidism
  • Tx: resect 3 1/2 glands or total parathryoidectomy and autoimplantation
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33
Q

Treatment: parathyroid Ca

A

Need radical parathyroidectomy (need to take ipsilateral thyroid lobe)

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34
Q

Treatment: primary hyperparathyroidism in pregnancy

A

Surgery in 2nd trimester; increased risk of stillbirth if not resected

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35
Q

What are benefits of intra op frozen section in primary hyperparathyroidism?

A

Can confirm that the tissue taken was indeed parathyroid

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36
Q

What are benefits of intra op PTH levels?

A

Can help determine if the causative gland is removed (PTH should go to

37
Q

Where do you check for missing glands in hyperparathyroidism?

A

Check inferiorly in thymus tissue (MC ectopic location, can remove tail of the thymus and see if PTH drops), near carotids, vertebral body, superior to pharynx, thyroid

38
Q

What if you still cannot find the parathyroid glands when you checked all ectopic locations?

A

Close and follow PTH; if PTH still increased, get sestamibi scan to localize

39
Q

At reoperation for a missing gland, where do you look?

A

The most common location for the gland is normal anatomic position

40
Q

What causes hypocalcemia post op in primary hyperparathyroidism?

A

From bone hunger or failure of parathyroid remnant / graft

41
Q

Hypocalcemia postop primary hyperparathyroidism: Normal PTH, decreased HCO3-

A

Bone hunger

42
Q

Hypocalcemia postop primary hyperparathyroidism: decreased PTH, normal HCO3-

A

Aparathyroidism

43
Q

Primary hyperparathyroidism: most commonly due to missed adenoma remaining in the neck

A

Persistent hyperparathyroidism (1%)

44
Q

What can cause recurrent hyperparathyroidism after surgery for primary hyperparathyroidism?

A
  • Occurs after a period of hypocalcemia or normocalcemia
  • Can be due to new adenoma formation
  • Can be due to tumor implants at the original operation that have now grown.
  • Need to consider recurrent parathyroid cancer
45
Q

Risks of reoperation in primary hyperparathyroidism

A

Associated with increased risk of RLN injury, permanent hypoparathyroidism

46
Q
  • Will have preferential uptake by the overactive parathyroid gland
  • Good for picking up adenomas but not 4-gland hyperplasia
  • Best for trying to pick up ectopic glands
A

Sestamibi scan

47
Q
  • Seen in patients with renal failure
  • Increased PTH in response to low Ca
  • Most do not need surgery (95%)
  • Ectopic calcification and osteoporosis can occur
A

Secondary hyperparathyroidism

48
Q

Tx: secondary parathryoidism

A
  • Ca supplement, vitamin D, control diet PO4, PO4-binding gel, decreased aluminum
  • Surgery for bone pain (MC indication), fractures, or pruritus (80% get relief)
49
Q

MC indication for surgery in secondary hyperparathyroidism

50
Q

What does surgery involve in secondary hyperparathyroidism?

A

Surgery involves parathyroidectomy with autotransplantation or subtotal parathyroidectomy

51
Q
  • Renal disease now corrected with transplant but still overproduces PTH
  • Has similar lab values as primary hyperparathyroidism (hyperplasia)
    Tx: subtotal (3 1/2 glands) or total parathyroidectomy with autoimplantation
A

Tertiary hyperparathyroidism

52
Q

Patients have increased serum Ca and decreased urine Ca (should be increased if hyperparathyroidism)

A

Familial hypercalcemic hypocalciuria

53
Q

What causes familial hypercalcemic hypocalciuria?

A

Caused by defect in PTH receptor in distal convoluted tubule of the kidney that causes increased resorption of calcium

54
Q

Dx: Ca 9-11, have normal PTH (30-60), decreased urine Ca

Tx?

A

Familial hypercalcemic hypocalciuria

Tx: nothing (Ca generally not that high in these patients); no parathyroidectomy

55
Q

Because of defect in PTH receptor in the kidney, does not respond to PTH

A

Pseudohypoparathyroidism

56
Q
  • Rare cause of hypercalcemia

- Increased Ca, PTH, and alkaline phosphatase (can have extremely high Ca levels)

A

Parathyroid Cancer

57
Q

MC location for metastases in parathyroid cancer

58
Q

Tx: parathyroid cancer

A

Wide en bloc excision (parathyroidectomy and ipsilateral thyroidectomy)

59
Q

5-year survival rate: parathyroid cancer

60
Q

Mortality in parathyroid cancer

A

Due to hypercalcemia

61
Q

Recurrence rate of parathyroid cancer

A

Recurrence in 50%

62
Q
  • Derived from APUD cells
  • Neoplasms can develop synchronously or metachronously
  • Autosomal dominant, 100% penetrance
A

Multiple endocrine neoplasia syndromes

63
Q

Components of MEN-one

A

Pituitary adenoma
Parathyroid hyperplasia
Pancreatic islet cell tumors

64
Q

Usually first part to become symptomatic in MEN one

A

Parathyroid hyperplasia

65
Q

Tx: parathyroid hyperplasia in MEN-one

A

4-gland resection with autotransplantation

66
Q

1 pancreatic islet cell tumor in MEN-one

A

Gastrinoma #1 - 50% multiple, 50% malignant; major morbidity of syndrome

67
Q

1 pituitary adenoma in MEN-one

A

Prolactinoma #1

68
Q

How do you begin to treat MEN-one?

A

Need to correct hyperparathyroidism 1st if simultaneous tumors

69
Q

Components of MEN-IIa

A

Parathyroid hyperplasia
Medullary CA of thyroid
Pheochromocytoma

70
Q

MC symptom of medullary CA of thyroid

71
Q

1 cause of death in MEN-IIa patients

A

Medullary CA of thyroid

72
Q

Usually first part to be symptomatic in MEN-IIa

A

Medullary CA of thyroid

73
Q

MEN-2a:

  • Nearly all patients; diarrhea most common symptom; often bilateral
  • # 1 cause of death in these patients
  • Usually 1st part to be symptomatic
A

Medullary CA of thyroid

74
Q

MEN-2a: often bilateral, nearly always benign

A

Pheochromocytoma

75
Q

How do you begin to treat MEN-2a?

A

Need to correct pheochromocytoma 1st if simultaneous tumors

76
Q

Components of MEN-2b

A
  • Medullary CA of thyroid
  • Pheochromocytoma
  • Mucosal neuromas
  • Marfan’s habitus, musculoskeletal abnormalities
77
Q

How do you begin to treat MEN-2b?

A

Need to correct pheochromocytoma 1st if simultaneous tumors

78
Q

Gene affected: MEN one

A

MENIN gene

79
Q

Gene affected: MEN2a and 2b

A

RET proto-oncogene

80
Q

Disease phenotypes related to mutation of the RET proto-oncogene

A

MEN2a (60%), MEN2b (5%), FMTC (35%)

81
Q

Germline mutations in cysteine codons of extracellular and transmembrane domains of RET

82
Q

Germline activating mutation in tyrosine kinase domain or RET

83
Q

Germline mutations in cysteine codons of extracellular or transmembrane domains of RET

84
Q

Causes of hypercalcemia

A
  • Malignancy
  • Hyperparathyroidism
  • Hyperthyroidism
  • Familial hypercalcemia hypocalciuria
  • Immobilization
  • Granulomatous disease (sarcoidosis or tuberculosis)
  • Excess vitamin D
  • Milk alkali syndrome
  • Thiazide diuretics
85
Q

Breakdown of hypercalcemia in malignancy

A
  • Hematologic (25%): lytic bone lesions

- Nonhematologic (75%): cancers that release PTHrP (small cell lung CA, breast CA)

86
Q

Inhibits osteoclasts (used with malignancies or failure of conventional treatment); has hematologic, liver, and renal side effects

A

Mithramycin

87
Q

Usually secondary to another surgery in patients with pre-existing hyperparathyroidism
- Tx?

A

Hypercalcemic crisis

Tx: fluids (normal saline) and furosemide (Lasix)

88
Q

How does breast cancer metastases to bone cause hypercalcemia?

A

Release PTHrP (rP = related peptide); can cause hypercalcemia

  • This is NOT due to bone destruction
  • Associated with increased urinary cAMP (from action of PTHrP on kidney)
89
Q

What do hematologic malignancy do to bone?

A

These can cause bone destruction with increased Calcium (urinary cAMP will be low)

ABSITE 2019-RM (33 decks)

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